Results 1 to 10 of about 5,435 (219)

Sodium channels and mammalian sensory mechanotransduction [PDF]

open access: yesMolecular Pain, 2012
Background Members of the degenerin/epithelial (DEG/ENaC) sodium channel family are mechanosensors in C elegans, and Nav1.7 and Nav1.8 voltage-gated sodium channel knockout mice have major deficits in mechanosensation. β and γENaC sodium channel subunits
Raouf Ramin   +7 more
doaj   +6 more sources

Subtype-Selective Small Molecule Inhibitors Reveal a Fundamental Role for Nav1.7 in Nociceptor Electrogenesis, Axonal Conduction and Presynaptic Release. [PDF]

open access: yesPLoS ONE, 2016
Human genetic studies show that the voltage gated sodium channel 1.7 (Nav1.7) is a key molecular determinant of pain sensation. However, defining the Nav1.7 contribution to nociceptive signalling has been hampered by a lack of selective inhibitors.
Aristos J Alexandrou   +27 more
doaj   +2 more sources

Sodium channels as a new target for pain treatment [PDF]

open access: yesFrontiers in Pharmacology
Voltage-gated sodium channels, especially the Nav1.7, Nav1.8, and Nav1.9 subtypes, play a crucial role in the transmission of pain signals. Nav1.7 is considered a threshold channel that regulates the generation of action potentials and is closely ...
Rui Chen   +6 more
doaj   +2 more sources

Nav1.8 and Chronic Pain: From Laboratory Animals to Clinical Patients [PDF]

open access: yesBiomolecules
As a subtype of voltage-gated sodium channel and predominantly expressed in the sensory neurons located in the dorsal root ganglion (DRG), the Nav1.8 channel encoded by the SCN10A gene is found to have different variants in patients suffering chronic ...
Yu-Feng Xie
doaj   +2 more sources

An approach to targeting Nav1.7 for pain sensations [PDF]

open access: yesThe Journal of Clinical Investigation
Pain is a serious medical condition with current treatments remaining limited by side effects. The Nav1.7 voltage-gated sodium channel is a crucial determinant of nociceptor excitability and a promising target for nonaddictive analgesics.
Theodore R. Cummins
doaj   +2 more sources

Mepyramine targets mutant Nav1.7 channels to relieve pain and erythema in primary erythromelalgia patients [PDF]

open access: yesFrontiers in Medicine
Gain-of-function mutations in SCN9A, which encodes the Nav1.7 voltage-gated sodium channel, are known to cause primary erythromelalgia (PEM). This condition is characterized by recurrent episodes of erythema, burning pain, and warmth in the extremities ...
Myriam Ducrocq   +9 more
doaj   +2 more sources

Learning molecular traits of human pain disease via voltage-gated sodium channel structure renormalization [PDF]

open access: yesComputational and Structural Biotechnology Journal
Mammalian neurophysiology vitally depends on the stable functioning of transmembrane, pore-forming voltage-sensing proteins known as voltage-gated sodium channels (NaVChs).
Markos N. Xenakis, Angelika Lampert
doaj   +2 more sources

Comprehensive Proteomic Profiling of Human Nav1.7-Interacting Proteins Reveals Conserved Regulatory Networks Involved in Nociceptive Signaling [PDF]

open access: yesNeuroscience Insights
The voltage-gated sodium channel Nav1.7, encoded by the SCN9A gene, is critically involved in the initiation and propagation of nociceptive signals. While prior research has delineated the interactome of mouse Nav1.7 (mNav1.7), the molecular partners ...
Xuelong Zhou, Jing Zhao
doaj   +2 more sources

Beyond CBD: Inhibitory effects of lesser studied phytocannabinoids on human voltage-gated sodium channels

open access: yesFrontiers in Physiology, 2023
Introduction: Cannabis contains cannabidiol (CBD), the main non-psychoactive phytocannabinoid, but also many other phytocannabinoids that have therapeutic potential in the treatment of epilepsy.
Carol J. Milligan   +11 more
doaj   +1 more source

E44Q mutation in NaV1.7 in a patient with infantile paroxysmal knee pain: electrophysiological analysis of voltage-dependent sodium current

open access: yesHeliyon, 2021
Gain-of-function mutations in voltage-gated sodium channels (NaV1.7, NaV1.8, and NaV1.9) are known causes of inherited pain disorders. Identification and functional assessment of new NaV1.7 mutations could help elucidate the phenotypic spectrum of NaV1.7
Kiichi Takahashi   +9 more
doaj   +1 more source

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